EMG Flashcards Preview

Medical and Applied Physiology > EMG > Flashcards

Flashcards in EMG Deck (18):

Describe the anatomy and physiology of muscles, as well as fine and gross movements

Voluntary Movements

•Fine motor movement: include ability to manipulate small objects and is controlled by Pyramidal system (includes pre-central gyrus (motor area), medulla ( fibers cross to the opposite side forming a pyramid) and descend to spinal cord),

•You are writing letter to friend. What part of nervous system are you using when pen move across paper ( is this gross or fine motor control?), where does the thought process originate?, where does the initiation of movement originate

Motor Areas

Gross Motor Movements

•use of LARGE muscles: activities controlled by extrapyramidal motor system ( origin at prefrontal cortex, but also in precentral, postcentral and temporal cortex). The descending fibers travel down spinal cord. Most fibers cross level of medulla.

•Q: What movements are defined as gross motor movements?

•Cerebellum is part of extrapyramidal system: role is to regulate and modify motor activities by receiving input and sending output to rest of brain and spinal cord.

Spinal Cord Mixed Nerves

•Ventral roots (motor/movement): bundle of motor neurons from ventral surface forms the ventral roots.

•Dorsal (sensory): each ventral root joins dorsal root to form spinal nerve which exits spinal cord through notches in vertebrae

•Called “Mixed spinal nerves” because they contain sensory and motor fibers.


Describe muscle contraction at the physical and molecular level

Muscle Contraction

•Motor unit: nerve, its axon & muscle fibers. Nerve from CNS can innervate between 3 (fine)- 3000 (gross postural adjustments) muscle fibres. Myofibrils contract in response to action potential sweeping down sarcolemma (plasma membrane surrounds the muscle fibres. Resting potential is -85 mV

•Skeletal muscles- innervated by myelinated neurons. Neuromuscular junction is in middle of muscle fibre. AP spreads from middle to ends and is brief but muscle contraction can last to 100msec.

•Tonus= maintained by steady flow of impulses from spinal cord to each motor unit. Atrophy with immobilisation (i.e. use it or lose it)

Myofibril Structure

•Actin (thin filaments), Myosin (thick filaments), Z-line (separates myofibril into segments.), Thin actin filaments have 2 regulatory proteins (tropomyosin and troponin).

•Muscle contraction occurs when thin filaments slide, along thick filaments and adjacent z line move towards each other.

Revision: Molecular Level

1.ACh released at neuromuscular junction

2.Voltage NA+ channel open in myofibril. Membrane depolarises and AP generated in muscle fibre, sweeps down sarcolemma to T tubules

3.Ca2+ released into sarcoplasm surrounding myofibrils from T tubules

4.Ca2+ binds to troponin and myosin binding sites are exposed

5.Myosin filaments take hold of actin filaments

6.Myosin heads rotates at expense of ATP

7.Actin filaments slide into spaces between myosin fibrils


Describe Electromyography- with a focus on noninvasive techniques

•EMG is technique measuring and recording electrical potentials associated with muscle fiber contraction.

•Invasive ( thin needle electrodes inserted to muscle tissues) used to examine limited muscle regions to study muscular disorders.). Detects disease of muscle itself ( muscular dystrophy in children), disease of neuromuscular junction, disease of nerves and nerve roots ( due to damage to nerve or ongoing nerve injury)

•Non Invasive surface EMG recorded from skin. Closer muscle to skin, stronger contractions and greater electrical activity. Most research work uses surface EMG recordings.

Electrode placement

•Clean skin via alcohol/ mildly abrasive material to remove dead skin, dirt and oil

•Electrode with electrode gel applied to skin (pregelled electrodes available ie. ECG)

•Electrodes must be washed in warm soapy water after use

•Bipolar placement of electrodes is common: both electrodes placed over muscle of interest. Resistance should be 500-10,000 ohms. Bipolar= more sensitive to variations in gradients of muscle activity between 2 electrodes.

•Monopolar method useful for low muscle activity site- one electrode over muscle of interest compared to electrode at site of low muscle activity. Monopolar electrodes= superior in picking up variations in absolute levels of electrical activity


Discuss the merits of needling vs surface recording techniques

Non-invasive EMG

•EMG is good indicator of tension in skeletal muscles

•EMG amplitude (uV) increases as handgrip strength increases ( using dynamometer) shown in earlier study

•Higher EMG amplitude produced by females to maintain a given grip level

Needling vs Surface Recording

•Diagnostic needle EMG used to study changes in motor unit morphology during effort in myasthenia gravis early on (Lindsey, 1930)

•Needline can be tolerated, has advantage of no increasing BP/ heart rate, irrespective of hypertension in patients

•Can be used in needle - guide botox injection in pathological conditions e.g. cervical dystonia, and its effects measured quantitatively by EMG

•Single- fibre EMG and jitter studies particularly useful in muscle disorders/diseases with young, the uncooperative persons with profound weakness

•However problems with non disposable needles for single fibre EMG, so ordinary concentric needles used which record from more than one fibre

•EMG with needling: pattern of muscle fibre recruitment and density of interference pattern can be quantified. There is linear relationship between mean power frequency and muscle fibre propagation velocity. Analysis of power spectrum of interference pattern is based on finding that there is greater power at high frequencies in myopathies and at low frequencies in chronic partial denervation. Well validated quantitative methods for assessing motor unit morphology and motor unit recruitment are now used extensively, and has been subject to authoritative reports & reviews ( Fuglsanf-Frediksen, 2006)

•Surface Recordings: practical and useful e.g. for ongoing background EMG, for long term recordings, to power prostheses or as control signal for computers and other devices. Stimulus evoked activity provides mainstay of most studies in motor control. Properties of motor unit including propagation velocity of muscle fibres can be probed in surface EMG recordings and recording can be decomposed to constituent motor unit potentials. However, surface recordings aren't selective- specific techniques required to minimise crosstalk ( Burke D, 2010).

•Abnormalities in EMG (both techniques) and nerve conduction help differentiate muscle disease (myopathy) from peripheral nerve (neuropathy) and neuromuscular jumction disorders. However they are used for other conditions/diseases

•NB. Muscle Biopsy, blood tests or immunoassays may be needed to confirm results


Be familiar with standardised electrode placements of EMG

Standardised Placement

•In bipolar recordings= electrode arrays consist of 2 active (placed along axis of muscle) and 1 inactive electrode (ground). Frontalis EMG and forearm EMG are standardised

•EMG signals need to be amplified (20-400Hz). Filtering systems must take this into account

•EMG= algebraic sum of all AP of fibres contracting between 2 electrodes


Discuss EMG and;
Behaviour- motor performance and reaction time

Motor Perf. & Reaction Time

•Davis (1940) recorded EMG from forearm extensor muscles while subject waited for signal requiring response. Muscle tension began 200-400 msec after signal. RT was faster the higher initial muscle tension was ( RT was quicker and muscle tension higher for periods vs irregular periods)

•Kennedy and Travis (1948) looking at tracking from frontalis muscle showed that RT become slower with low levels of tension and faster with high tension level

•Non involved muscles show low EMG activity- this is linked with decreases in HR ( cardiac- somatic concept)


Discuss EMG and tracking

•Tracking- movement of control to indicate moving target. I.e. video games and pilots

•Efficient tracking= related to moderate to high EMG level. Low muscular tension ( indicate drowsiness), or high ( overexertion/fatigue) are associated with less efficient performance

•Practice= improves tracking. Simple repetition without fatigue improves performance

•Motivation= facilitates performance. Fatigue hinders it (Eason and White). Fatigue causes integrated EMG levels to increase but muscle efficiency to decrease


Discuss EMG and Speech

•Oral EMGs occur during thinking ( not confined to larynx). Speech muscles are separate ( Goldestein 1972): “muscle activity accompanies all cognitive phenomena, even though EMG may be of small magnitude” (McGuigan 2973)

•Sub vocalisation during reading limits reading rate to 150 words/min, Hardyck et al (1966) found 17/50 subjects were sub vocalisers

•Audio EMG feedback of laryngeal muscles *- within 30 min. All able to read with EMG at resting levels. Reductions in reading fatigue occurred.

•Mcguigan (1973) in a contrasting view suggested that higher levels of oral EMG in children and less proficient adults enhances comprehension levels, and reduces distractions in noisy environment


EMG and performance

EMG & Performance

•Max effort can be maintained only 1 min. 25% of max for approx. 10 min. Efficiency decreases when high level of exertion required

•Maintaining performance under fatigue requires more energy ( higher level of EMG). 20min pencil paper test doing addition problem

•Normal sleep vs 32-56 hr sleep deprivation

•After sleep loss, EMG from inactive forearm show those with greatest increases in EMG over normal levels, performed best (Wilkinson 1962)

•Desk slant position (Eastman and Kamon, 1976)

•EMG was recorded from deltoid, trapezius and spinae erector (lower back ) while subjects performed reading and writing tasks at 12 and 24 degree desk tlits. Work stations can therefore be redesigned


EMG and mental activity

EMG during Mental Activity

•Operant conditioning of EMG: Hayes 1975- used EMG auditory feedback of muscle tension Group 1 vs controls:

•EMG auditory feedback of muscle tension (group 1)

•Active or passive relaxation, Group 2 ( get verbal instructions)

•No assistance group (told to be as relaxed as possible) Group 3

•Noncontingent feedback in form of random tone (group 4)

•EMG biofeedback group achieve greater degree of muscle relaxation than either of relaxation groups and much greater than controls

However lowering EMG level in one muscle ( eg. frontalis) does not generalise to other muscles

•But can show classical conditioning ( recording EMG from masseter and forearm muscles) in experiment

•Experimental group, with conditioned stimulus (CS) gets an audio tone and an unconditional stimulus (USC) a different tone vs.

•Control group which only get conditioned stimulus CS

•Experimental group show larger EMG to CS than control group, indicates conditioning of muscle being recorded ( Pavlovs dog experiment with Bell CS and meat USS)


EMG and Emotion

EMG & Emotion

•Facial EMG ( Schwartz & collegues 1970s) found different muscles responsible for different facial expressions: Corrugators knit brows, triangularis depresses mouth, Zygomatic gives smiles.

•Using pleasant or unpleasant imaging : Fridlund & cacioppo (1986) presented guidlines for electrode placements in facial EMG research

•Contralateral control (RHS is more active ) : RHS of brain active in spontaneous emotional response. I,e, LHS muscles show increased activity.

•Individuals exposed to happy and angry pictures of facial expressions showed different responses. Happy picure increased zygomatic activity, angry faces elicited corrugator activity ( Dimber 1982)

•Measure of mood and EMG show feelings of elation and depresseion were elicited in 70% of subjects. Elation increased zygomatic activity and depression increased corrugator activity ( Sirota and Schwartz 1982)

•Has been hypothesised that facial muscle play role as feedback system for experience of emotion. Original proposal by Darwin that facial expressions= biologically pre wired and consistent between individuals

•Gender difference: women show more pronounced EMG response in zygomatic and corrugator muscles. Female more expressive than males ( Dimberg 1997)

Anger In and Out

•Is there a difference in outward/ inward expression of anger?

•Jancke 1996- measured frontalis, corrugator, orbicularis oculi, sygomatic EMG. All subjects asked to complete IQ test. Control group given neutral feedback, thanking them for study. Experimental group told score was too low and no payment would be given. Subjects who expressed anger outwardly had higher frontalis and corrugator activity.

•EMG displays serve a social communication purpose rather than reflecting felt emotions


Repetitive strain injury

Repetitive strain injury

•Repetitive movement associated with repetitive motion disorders (RMDs)- chronic overuse condition affecting muscles, nerve. Joint leading to inflammation or pain 9 Fuller et al., 2008)

•Repetitive arm movements- major facet of several workplace task ( e.g. manufacturing, assembly line work, services, sports and leisure activities)

•During sustained maximal contraction, fatigue ( reduced functional capacity) is observed as decline in force output

•Effects of fatigue on muscle output show as compression of power spectrum toward lower frequencies in EMG due to reduced motoneuronal excitation

•Other studies show increase in EMG amplitude ( e.g root mean square of RMS values) concomitant to decreases in frequency characteristics with fatigue development during submaximal contractions

•Study of mechanisms of low force muscle fatigue show selective fatigue of low threshold motor units during sustained wrist extensions and change in physiological parameters ( IL-6, muscle lactate, K+, local tissue oxygenation, total Hb) at NMJ of trapezius muscle during low load repetitive tasks

•In addition, gender differences in various aspects of fatigue response mechanisms (e.g. endurance time, strategies of muscle adaptation) recently documented


Myasthenia Gravis

EMG & Neuromusc. Disorders

Myasthenia Gravis

•Autoimmune disease- caused by antibody mediated loss of ACh receptors at NMJ and thus loss communication between motor neuron and muscle

•Peak incidence 20-30 yrs, 3x more common in women, in later life more men affected

•Weakness in muscle for chewing, swallowing and limb movements- more pronounced in proximal than distal parts thus difficulty climbing stairs and lifting objects

•Weakness and fatigue with sustained muscle effort

•Eye and periorbital muscle most commonly affected- ptosis- drooping upper eyelid and diplopia- double vision

•Lower facial muscles and speech thus impaired later in disease. Myasthenia crisis ( due to stress, illness, pregnancy, post surgery) when weakness severe to compromise ventilation- need artificial ventilation

•Muscle weakness can be detected by single fibre EMG: detects delayed or failed neuromuscular transmission in muscle fibres supplied by single nerve fibre. Can be confirmed by immunoassay tests (detect presence of ACh receptor Ab in blood)



•Degenerative disorder of basal ganglia function

•Specifically degeneration of dopamine producing fibres in substantia nigra

•Results in variable combination of tremor, rigidity and bradykinesia ( hypokinesia)

•Bradykinesia- slowness in performing and starting movement, difficulty in sudden and unexpected stopping of voluntary movements

•Patients lean forward to maintain centre of gravity.

•Use surface EMG signals to discriminate parkinson tremor from essential tremor (ET- relatively benign disease with tremor being main sympto,/ also used in diagnosis when hypokinesis first appears)

•Research indicate genetic component in early onset form of parkinson's disease

•Theory- autoxidation of catecholamines e.g. dopamine, during melanin synthesis injures neurons in substantia nigra

•Increase evidence that disease development may be due to accumulation of toxic metabolites that neurons cannot render harmless

•Latter due to disruption of mitochondrial electron transport system which usually inactivates metabolites

•Those with family history have gene mutations: park1, sometimes Park2 but rarely)


Lower Back Pain & Pelvic Floor Muscle tone

•LBP- common condition worldwide, ranked as 1st cause of disability and inability to work in USA

•Overall mechanical stability of spinal column, especially in dynamic conditions and under heavy load, is provided by spinal column and precisely coordinated surrounding muscles

•Australian longitudinal study on women= those with preexisting incontinence, gastrointestinal problems and breathing disorders- more likely to have LBP than women without

•This was a result of changes in control of trunk muscles following involvement with incontinence, respiratory and gastrointestinal problems

•Changes in morphology and altered postural activity of the trunk muscles including muscles of respiration and continence ( provide mechanical support to spine and pelvis) shown related to LBP

•EMG of coactivation pattern of pelvic floor and abdominal muscles ( needle EMG for abdominals & surface EMG for pelvic floor muscles PFM, found): abdominals contract responding to pelvic floor contraction command. Pelvic floor contracts responding to both a hollowing and bracing abdominal command

•Thus pelvic floor can be facilitated by co activating abdominals and vice versa. Also increasing abdominal muscle EMG activity result in increasing EMG activity in PFM


Rheumatoid Arthritis

•Chronic inflammatory disorder mainly affects synovial joints

•Symptoms include loss of extension of digits or droooed finger

•Cause ~ loss of normal muscle function associated with subluxation of ulna and of extensor tendons over hand joints & dislocation of MCPJs

•Posterior interosseous nerve (PIN) palsy, with loss of digital extension is rare neurological complication of RA. Cause~ nerve entrapment, vasculitis, or drug toxicity

•Diagnosis of PIN Palsy may be confirmed by electrophysiological studies (includes EMG)

•EMG results help treatment options medial/drug therapy or surgery


EMG Behaviour & Emotion

•Threatening facial expression - an ancient sign of threat in human evolutionary history

•Social phobia= mental dysfunction relevant to threatening faces

•Socially anxious individuals concerned with humiliating themselves when under scrutiny

•Threatening expression - sign of disapproval and rejection, thus function as anxiety provoking cue in people who seek approval

•People with social phobia form negative assumptions about how others see them causing attentiveness to threatening environmental cues

•Facial EMG measures “valence dimension: or strength of emotions.

•Hypothesis- a biological predisposition to react to emotional faced will manifest itself in a facial mimicry that can be measured with EMG

•More specifically, larga facial muscles, Zygomaticus major (controls smiling), corrugator supercilii ( controls frowning) should show increased activation in response to happy and angry faces respectively

•Some studies- increased corrugator activity (frowning) to angry faces in high, compared to low socially anxious participants whereas others found no group differences in response to angry faces

•Studies found effect specific to angry faces, used long (100ms) exposure durations, while others presented stimuli until participant response. This difference in exposure duration appears to be crucial

•Higher levels of social anxiety within clinical population linked to more pronounced avoidance of angry faces compared to patients with lower levels of social anxiety


EMG & Stuttering

•Neurophysiological processing of speech fluency depend on stability of temporal coordination between motor execution and performed cognitive processing

•Developmental stuttering- communication disorder begin in early childhood ( 3-6 yrs)- involuntary disruptions in fluency of verbal expression

•Hypothesis~ stuttering due to many factors: temporal disruption of simultaneous and successive programming of muscular movements: error in sequencing the normal motor command leading to delay in production of sound, anticipatory, apprehensive, hypertonic avoidance reaction an extraneous muscle activity, the result of deficiency in speech motor skill such as disorder in coordination of different muscle systems ( respiratory, circulatory or laryngeal) or slower retrieval of speech motor plans

•Typical - repetition of sounds or syllables, articulatory fixation, resulting in blocks or prolongation of sounds

•High EMG levels shown in lower orbicularis oris muscle at time of speech onset and during speech production

•Studies focus on EMG of lip muscle are controversial, other studies ~ stuttering not associated with unusually high levels of muscle activity in lip muscles

•De Felicio 2007- study on upper and lower lip muscles to compare stutterers from fluent speakers with EMG

•Note; stuttering recognised genetic component 9 supported by twin and adoption studies)- approx half all stutterers have family history, transmission unknown

•EMG study (defelicio et al 2007) on stuttering noted: activity upper lip lower in stutterers than control in some clinical conditions, there was no difference in lower lip activity between stutterers and controls, results don't confirm subjects who stutter present high levels of muscle activity in lip muscles than fluent speakers.

•Finding include resting activity, do not confirm stuttering as hypertonic avoidance reaction or as extraneous muscle activity.

•No evidence that stutterers during fluent speech, present increase in lower lip muscle activity compared to non stutterers

•Abnormal aspect of EMG is actually tremor in orofacial and laryngeal muscles during disfluencies